NUR 305 Neurological Disorders II

Increased Intracranial Pressure (Intracranial Hypertension)

Increased intracranial pressure due to increased volume in the cranial.

• Inc vol in cranium → Inc ICP

• When blood escapes vasculature, inflammatory response occurs, causing leaky vessels that cause swelling/edema.

Brain occupies 80% of the skull

• CSF and blood vol. make up other 20%.

Monro-Kelli Hypothesis

• Volume increase in brain is compensated for by shifts in CSF & blood volume.

• CSF and blood gets shifted out, blood vessels constrict.

Monro-Kellie Hypothesis

Increase in volume of one component must be compensated by a decrease in volume of another.

Difference between Adult and Child Skull

Adult Skull

• Rigid, does not expand.

Child Skull

• Softer.

• The fontanelles close by age 3 years usually (skull can expand somewhat)

Causes of Increased Intracranial Pressure

1. Cerebral Edema

2. Inflammation

3. Traumatic Brain Injury

4. Brain Tumors

5. Hydrocephalus

6. Intracranial & Intracerebral Hemorrhage

Cerebral Edema (Causes of Increased Intracranial Pressure)

• 3 types — Vasogenic, Cytotoxic, Interstitial

Inflammation (Causes of Increased Intracranial Pressure)

• Blood vessels become permeable, “leaky”, leading to edema.

• Contusions may cause damage/necrosis.

Traumatic Brain Injury (Causes of Increased Intracranial Pressure)

• Can lead to inflammation or bleeding (cerebral hemorrhage).

• Blunt or penetrating injury.

Brain Tumors (Causes of Increased Intracranial Pressure)

• Excess tumor tissue changes the equilibrium of the ICP’s components.

  • Occupies space.

• Compresses vessels → diminishes blood flow → venous congestion & increased hydrostatic pressure → edema.

  • Walls of veins are weaker than arteries.

• Can be caused by benign or malignant tumors.

Hydrocephalus (Causes of Increased Intracranial Pressure)

• Occupies space.

• Accumulation of excess CSF — forms blockages/slowing of drainage of CSF — Usually in the 3rd ventricle.

• CSF fluid overload is specific to Hydrocephalus.

Intracranial/Intracerebral Hemorrhage (Causes of Increased Intracranial Pressure)

• Blood that forms a space-occupying lesion within the closed cranium.

• Blood is toxic to brain cells and places pressure on brain tissue, which rapidly increases ICP.

  • Toxicity causes inflammatory response.

Vasogenic Cerebral Edema

• Caused by trauma and shearing stress.

• Occurs due to changes in the volume of brain tissue.

• Cerebral vessel walls have abnormal permeability which allows protein-rich plasma to leak into the extracellular space of the brain.

Cytotoxic Cerebral Edema

• Result of a hypoxic injury.

• Caused by cardiac arrest, unrelieved respiratory distress and failure, shock.

• Brain is depleted of oxygen.

  • Begins using anaerobic metabolism.

• Sodium pump fails.

  • Sodium enters the cell and pulls water with it.

  • Results in an abnormal accumulation of fluid in the brain cells.

Interstitial Cerebral Edema

• Occurs with acute brain swelling.

• Severe hypertension.

  • Leads to hypertensive stroke.

• Associated with elevated blood pressure or increased CSF pressure.

• Must lower BP, decrease CSF pressure, or increase the CPP >70 mmHg.

Diagnosing Intracranial Hypertension (Intracranial Pressure)

1. History & Physical Exam

   • Neuro issues, congenital vs. acquired.

2. Glasgow Coma Scale

   • V/S, Pupillary response

3. Head CT

4. MRI

   • Better to inspect smaller bleeds.

Treatment for Intracranial Hypertension (Intracranial Pressure)

Depends on the cause (bleed, tumor, hydrocephalus, meningitis).

General Treatment

1. Rest the brain

   • Any noxious stimulus can exacerbate ICP.

2. Prevent increases in ICP

   • Limit coughing.

3. Prevent complications

   • Prevent bed sores.

   • Keep HOB at 30-45 degree angle (keeps ICP stable)

   • Keep neck neutral (prevents blood flow from getting blocked).

Manifestations of Intracranial Hypertension (Intracranial Pressure)

• Decreasing level of consciousness.

• Vomiting (often projectile).

• Rising blood pressure (compensation).

  • Makes sure there is adequate perfusion to the brain.

• Increasing pulse pressure.

  • SBP-DBP = Pulse Pressure

• Bradycardia.

• Papilledema.

  • Look at optic disc → Diffuse look is inflammation = Inc ICP

  • Swelling around the optic nerve.

• Fixed and dilated pupils.

• Posturing.

  • Decorticate (to the core). Brings limbs inwards toward body.

  • Decerebrate is worse. Bends limbs outwards away from body.

Cushing's Triad (Increased ICP)

A late sign of intracranial hypertension, indicates impending herniation.

1. Increased blood pressure.

2. Bradycardia

3. Cheyne-Stokes respiratory pattern.

What are the compensatory mechanisms to Cushing’s Triad?

1. Autoregulation

2. Cushing’s Reflex

Autoregulation (Compensatory → Cushing’s Triad)

Involves the aortic arch and baroreceptors.

The blood vessels either:

• Dilate to increase blood flow

• Constrict if ICP increases.

This only acts up to a certain point.

Cushing's Reflex (Compensatory → Cushing’s Triad)

The hypothalamus increases sympathetic stimulation when the mean arterial pressure drops below the ICP.

• MAP < ICP

Causes:

• Vasoconstriction in the periphery.

• Increased cardiac contractility.

• Increased cardiac output.

These mechanisms increase perfusion to the brain.

Herniation

• Feared complication of increased ICP.

• Refers to displacement of brain tissue.

• Can be fatal quickly.

In Transtentorial (Central) Herniation

Leads to Impairment In:

• Cerebral blood flow

• CSF

• Reticular Activation System

• Respirations

Uncal Herniation

Puts Pressure On:

• Cranial Nerve III

• Posterior Cerebral Artery

• Reticular Activation System

Cerebellar or Tonsillar (Intrafratentorial) Herniation

Compresses the brain stem and vital centers, causing death.

Hydrocephalus

• Excess CSF accumulation within the skull.

• Causes pressure on cerebral blood vessels and brain tissues.

• Usually occurs in the narrow 3rd ventricle.

• CSF flow becomes blocked or poorly reabsorbed.

• Often fatal if left untreated.

Risk Factors of Hydrocephalus

• Pregnancy-related problems

• CNS abnormalities

• Illness

• Tumors

  • Especially in adults

  • In brain or spinal cord

Manifestations of Hydrocephalus in Infants

• Increase in head size

• Bulging fontanel

• Vomiting(often projectile)

• Lethargy, irritability, high-pitched cry (pain!)

• Feeding difficulties

• Seizures

• Eyes that gaze downward

• Development delays if untreated

Manifestations of Hydrocephalus in Older Children and Adults

• Signs & symptoms same as those for increased ICP

• These changes can progress to urinary incontinence and self-care deficits.

Diagnosing Hydrocephalus

• History

  • What happened during the pregnancy?

• Physical examination

• Skull X-rays

• CT

• MRI

• Prenatal Ultrasound

Treatment of Hydrocephalus

1. Surgery to repair the blockage.

2. Ventriculoperitoneal (VP Shunt) Placement.

   • Surgical procedure that diverts excess cerebrospinal fluid (CSF) from the brain's ventricles into the abdominal cavity.

T/F: Hypertonic Solutions are effective for treating hydrocephalus.

False; Hypertonic solutions are not effective for treating hydrocephalus.

Why are hypertonic solutions not effective for treating hydrocephalus?

1. CSF flows AROUND the brain and spinal cord.

2. Hypertonic solutions work by drawing fluid through osmotic action across the blood-brain barrier into the intravascular space (ie. Bloodstream).

3. CSF does not flow through each neuron, but instead serves as a cushion for the brain and spinal cord.

4. Nutrients move from CSF into cells but CSF DOES NOT FLOW THROUGH THE BRAIN TISSUE ITSELF.

Traumatic Brain Injury (TBI)

A traumatic insult to the brain possibly producing physical, intellectual, emotional, social, and vocational changes.

Causes

• 50% are motor vehicle accidents.

• 21% are falls.

• Others: Violence and Sports

What are the types of TBIs?

General

1. Blunt

2. Concussion

3. Open Trauma

4. Focal

5. Coup (Whiplash effect)

6. Contrecoup (Whiplash effect)

Fractures

1. Linear Skull Fractures

2. Comminuted Skull Fractures

3. Depressed Skull Fractures

4. Compound Fractures

5. Basilar Skull Fractures

Blunt (Closed) Trauma (TBI)

• The dura remains intact.

• Brain tissues not exposed.

• Include:

  • Focal (local) brain injuries.

  • Diffuse (general) brain injuries.

Open (Penetrating) Trauma (TBI)

• Injury breaks the dura.

• Exposes the cranial contents.

• Risk of infection is high.

• Ex) Gunshot wounds.

Concussion (TBI)

Momentary interruption of brain function.

Signs/Symptoms (Depends on Severity)

• Amnesia

• Confusion

• Sleep disturbances

• Headaches that may occur for weeks or months.

Focal Injuries (TBI)

Localized to the site of impact.

Coup Injury (TBI)

Injury directly below the point of impact.

Contrecoup Injury (TBI)

Injury on the pole opposite the site of impact.

Compound Fractures (TBI)

Open fracture, going through the skin.

Basilar Skull Fracture (TBI)

• Fracture at the base of the skull.

  • Extending into the anterior, middle, or posterior fossa.

• Results in CSF leakage from nose or ears.

  • Check if glucose is present in drainage from nose/ears → If glucose present = CSF

• Battle’s Sign

  • Mastoid area bruising indicates basilar skull fracture.

Linear Skull Fracture (TBI)

Simple clean break in skull.

Comminuted Skull Fracture (TBI)

Fragmentation of bone in skull.

Depressed Skull Fracture (TBI)

Bone is pressed inward into the brain tissue.

Complications of Skull Fractures

Infections and Disability

Manifestations of TBI (Physical)

• Fracture of skull/face

• Scalp wound

• Swelling of injury site

• Facial bruising

• Rhinorrhea

  • Clear nasal drainage.

• Otorrhea

  • Clear drainage from the ears.

• Pupil changes

  • Unequal pupil size (Rising ICP)

Manifestations of TBI (Neurological)

Seizures

Inability to recall event details

Irritability

Personality changes

Unusual behavior

Restlessness

Loss of consciousness

Poor coordination

Loss of movement

Lethargy

Stiff neck

• Positive Brudzinski’s sign

• Meningeal irritation

Slow respirations (bradypnea)

• Look out for Cushing’s Triad

Hypotension

Vomiting

Impaired hearing, smell, taste, speech, or vision

When examining for Neurological TBI Manifestations, what should the nurse consider?

• Meningeal irritation and increased ICP.

• Slow respirations and hypotension may indicate Cushing’s Triad.

Diagnosing TBIs

• History & Physical Exam

  • What happened?

  • Neuro Exam

• Glasgow Coma Scale

• Head CT or MRI

  • MRI allows for more detail to be seen (like small bleeds) that cannot be captured by CT.

• ICP Monitoring

  • Placed surgically to monitor ICP

  • Goal range (5-15mmhg)

Treatment for TBIs

1. Rest the Brain!

   • Decrease stimuli

2. Reduce Cerebral Edema

   • Osmotic diuretics

   • Ex) Hypertonic 3% NaCl, Albumin, Mannitol

   • Pulls fluid from brain into vasculature

3. Decrease Energy Expenditure

   • Sedatives

4. Control Fever

   • If uncontrolled, can lead to brain damage

5. Prevent Seizures

   • Can lead to brain damage.

Acute TBI Management

1. ABCs (airway, breathing, circulation)

2. Assessment of vital signs to detect increased ICP

   • Prevent Cushing's triad!

3. Reduce/Prevent Increased ICP

How can the nurse help Reduce/Prevent Increased ICP during Acute TBI Management?

1. Positioning

   • Avoid Trendelenburg position → Causes Inc ICP

   • Avoid bearing down → Causes Inc ICP

2. Keep neck in neutral position

   • Avoid lateral twisting/turning head to the side.

     • May block blood flow to brain.

3. Prevent buildup of secretions in the lungs.

   • Encourage pt. to cough.

4. Maintain homeostasis

   • Ensure optimal body functions, vital signs, arterial blood gases, etc…

5. Prevent Complications

   • Pneumonia

   • Infections

   • Decubitus ulcers

TBI Complications

• Changes in thinking, sensation, language, or emotions

  • Long-term

• Seizures

• Memory decline

• Depression

• Concussions

• Alzheimer’s disease

• Parkinson’s disease

What are the 4 arteries that perfuse the brain?

• 2 Posterior Vertebral Arteries

• 2 Anterior Carotid Arteries

TBI Prevention

• Seat belt use

• Appropriate child safety seats

• Helmets (sports, biking, skating)

• Home safety (prevent falls, injuries)

  • Elderly population.

  • Furniture, rugs, safety bars in bathroom.

• Storing firearms in locked cabinets

• Never driving impaired/distracted

  • Phone or drugs.

• Child supervision

Cerebral Hematomas/Bleeds

• A collection of blood or a clot in an area inside or near the brain.

• Left untreated may lead to inflammation and increased intracranial pressure.

• Can lead to severe neurological injury or death.

What are the 4 types of Cerebral Hematomas/Bleeds?

1. Epidural

2. Subdural

3. Intracerebral

4. Subarachnoid

What are the differences between the 4 types of Cerebral Hematomas/Bleeds?

1. Epidural

   • Arterial bleeding into space between dura and inner table of skull.

2. Subdural

   • Bleeding between the dura and arachnoid space.

3. Subarachnoid

   • Bleeding between the arachnoid space and pia.

4. Intracerebral

   • Bleeding in the brain tissue itself.

What methods can the nurse use to control Cerebral Hematomas/Bleeds?

• Respiratory Support

  • Semi-Fowler's positioning

  • Decreases edema, swelling.

• Prevent Seizures.

• Reduce brain metabolism.

• Limit activities that increase ICP.

• Control glucose level.

• Stress ulcer prevention.

Diagnosing Cerebral Hematomas

• History and Physical Exam

• Glasgow Coma Scale

• Head CT, MRI

• Cerebral Angiogram

  • Tracking vasculature of blood vessels in the brain w/ IV dye.

• ICP monitoring

Treatment for Cerebral Hematomas

Surgical removal of the blood through a burr hole or a craniotomy.

• Burr Hole = Drill hole in head to relieve pressure/drain blood.

• Craniotomy = Take a piece of skull plate out.

Physical, speech, and occupational therapy.

• Damage and ischemia may impair these functions.

• Once O2 comes back, these functions may return.

  • Plasticity

Same treatment as for increased intracranial pressure.

Epidural Hematoma

Neurologic emergency with potentially catastrophic ICP elevation.

Caused By

• Arterial bleeding into space between the dura and inner table of skull.

  • Most common cause.

• Temporal bone fractures.

• Tearing of the middle meningeal artery.

  • Common cause

What is an Important Sign of an Epidural Hematoma?

Momentary unconsciousness follows lucid interval within minutes of injury.

Subdural Hematoma

• Bleeding develops between the dura and arachnoid space.

• Frequently caused by a small venous tear.

  • Bleeds slower than an arterial tear b/c venous system is a lower pressure system.

• Acute and Chronic types.

• ICP increases over a period of about a week after the injury.

Acute Subdural Hematoma

• Develops within 24 hours of injury.

• Progresses rapidly.

• Has a high mortality rate.

Chronic Subdural Hematoma

• Develops several weeks after the injury due to slow leak.

• More common in elderly adults because of brain atrophy.

Subarachnoid Hemorrhage

Bleeding in the space between the arachnoid and pia.

Causes

• Most are from arterial bleeding.

  • 80% are from ruptured cerebral aneurysms

  • 20% are trauma induced.

Risk Factors for Subarachnoid Hemorrhage

• Hypertension

• Cigarette smoking

• Family history

• Alcohol abuse

• Sympathomimetic drugs

• Estrogen deficiency

• Older age (>60 years)

• Posterior circulation location

• Atherosclerosis

• Large Intra-arterial aneurysm (IA) size (>5 mm)

• Autosomal dominant polycystic kidney disease

Symptoms of Subarachnoid Hemorrhage

Classic

• Sudden, severe headache, worse in the back of the head (occiput).

• * “Worse headache of my life!” *

Other

• N/V

• Dizziness

• Orbital (eye socket) pain

• Diplopia

• Visual loss (occiput)

Meningeal

• Positive Brudzinski’s

  • Specific to meningeal irritation.

• Possibly Kernig’s due to spread of blood down the 4th ventricle.

  • Blood gets into CSF

  • Indicates disc disease.

Management of Subarachnoid Hemorrhage

Control blood pressure

• Administer anti-hypertensive medications to keep MAP <130mmHg.

Osmotic Diuretics and/or Hypertonic Solutions

• These medicines reduce cerebral edema.

Treatment for Subarachnoid Hematoma

Surgical treatment to prevent rebleeding.

• Clipping

• Coiling

The choice between coiling and clipping usually depends on:

• The location of the lesion.

• The neck of the aneurysm.

• The availability and experience of hospital staff.

Complications of Subarachnoid Hematoma

• Hydrocephalus

• Brain Herniation

• Vasospasm

  • Receptors are off

  • Repeated Vasodilation/Vasoconstriction

• Seizures

• Hyponatremia

  • Loss of Na+ through urine.

  • Exacerbates cerebral edema.

• Pulmonary & Cardiac

  • Issues of control w/ brain and heart.

MAP Calculation

MAP = [(2 x diastolic)+systolic] / 3.

Intracerebral Hematomas

Bleeding in the brain tissue itself.

Causes

• Contusion or shearing injuries.

• Hypertension

  • Hypertensive Crises

• Cerebral/Vascular Accidents (CVAs)

  • Strokes

• Aneurysms

  • Often congenital

• Arterio-venous malformations (AVMs)

  • An abnormal/malformed connection between arteries and veins.

    • Causes weakness in connection, can burst.

Management of Intracerebral Hematomas

Depends on the cause and the severity.

• Prevent/Reduce cerebral edema.

• Control blood pressure.

• Surgical for space occupying bleeds.

• Conservative treatment for small bleeds.

Complications of Intracerebral Hematomas

• Hydrocephalus

• Seizures

• Rebleeding

• Vasospasm

• Brain herniation

Transient Ischemic Attack (TIA)

Warning signs of stroke.

Transient and focal (localized) neurologic dysfunction.

• Most commonly occurs in the face.

Causes

• Brief interruption in cerebral blood flow

  • Resulting from cerebral vasospasm or systemic arterial hypertension.

T/F: A patient with reversible ischemic neurologic deficit has signs and symptoms that look just like a stroke (paralysis, weakness, numbness, loss of speech) except that these symptoms will go away within a week.

False; These symptoms go away within 24 hours.

Stroke (Cerebrovascular Accident (CVA))

• A change in the normal blood supply to the brain.

• Two Types

  • Ischemic

  • Hemorrhagic

• Treatment of CVA depends on which type it is.

Why is a CVA (Stroke) life-threatening?

• The brain is unable to store oxygen or glucose and must receive a constant flow of blood to function.

• Strokes restrict adequate blood flow throughout the brain through blockage of blood flow or intense cerebral bleeding.

Ischemic Stroke

Stroke caused by a blockage:

• Thrombotic = Stationary blood clot.

• Embolic = Blood clot that travels.

Both types of blockages block blood flow to an area of the brain.

Hemorrhagic Stroke

A CVA that occurs due to immense bleeding.

Causes

• Ruptured cerebral aneurysm.

• Arteriovenous malformation (AVM) bleeding

When a clot is “thrombotic,” what does this mean?

The clot is stationary.

When a clot is “embolic,” what does this mean?

The clot is traveling throughout the body.

Risk Factors for CVAs

Populations

• African Americans

• Those living in the Southeast.

Lifestyle

• Hypertension

• Smoking

• Inactivity

• Obesity

• High Cholesterol

• Diabetes

• Atherosclerosis

• Oral Contraceptive use

  • Increases risk of blood clots.

• Alcohol abuse

• Illicit drug use

Arterial Fibrillation

Irregular and very rapid heart rhythm.

• Can lead to blood clot formation → become emboli → cause embolic CVA.

Symptoms of an Aneurysm Rupture

• A sudden severe headache

• Increased ICP

FAST Stroke (Signs and Symptoms of a Stroke)

Face

• Ask pt. to smile.

• Facial drooping on one side = pos. finding for CVA

Arms

• Ask pt. to raise both arms.

• Weakness or paralysis in one arm = pos. finding for CVA

Speech

• Ask the pt. to repeat a simple phrase.

• Difficulty speaking = pos. finding for CVA

Time

• Call 911

• Clock starts ticking from the FIRST clinical manifestation.

• Only 3 hours available to receive treatment to reverse neurological deficits.

• After 3 hrs, permanent damage occurs.

Complications Immediately After the Stroke

• Cerebral edema

• Increased intracranial pressure

• Dysphagia

• Seizures

Stroke Complications Related to Immobility

• Hydrocephalus

• Vasospasms

• Rebleeding or rupture

• Bed sores

Meningitis

Inflammation of the meninges (usually infectious).

What causes Meningitis?

The following causes trigger the inflammatory process, leading to swelling of the meninges and increased ICP.

Bacteria (Can be Quickly Fatal)

• Neisseria meningitidis

• Streptococcus pneumoniae

• Haemophilus influenza

Viruses

• Enterovirus

• Measles

• Influenza

• Herpes

Other (Rare)

• Tumors

• Allergens

Meningitis Risk Factors

Age

• <25 y.o (frequent community settings)

• Infants (immature immune system)

Community Settings

• Schools

• Institutions

Certain Medical Conditions

• Immunosuppressed individuals.

Travel to Endemic Regions

• Sub-Saharan Africa

Meningitis Signs and Symptoms

S/S

• May present with sudden onset of fever, headache, and stiff neck.

  • Stiff neck = Positive Brudzinki

• Nausea

• Vomiting

• Photophobia

• Altered mental status-confusion

Development of S/S

• Typically develops 3-7 days after exposure

• Can appear suddenly or over several days.

Diagnosing Meningitis

• History

• Physical examination

  • Test Brudzinski’s

• Throat cultures

  • Strep

• Lumbar puncture with CSF analysis

  • If CSF cloudy = high WBC count = definitive for infection

• PCR test

  • Polymerase chain reaction test

  • Tests DNA of infecting agent

• Head CT

Treating Meningitis

Treatment

• Antibiotics (if bacterial)*

• Antiviral (if viral)*

• Hydration

• Fever management

Prevention

• Vaccination (MCV4 series)

  • Meningococcal Conjugate Vaccine

  • Consists of 4 injections spread out through childhood and adolescence.

*Medications must be able to cross the blood-brain barrier.

Encephalitis

Inflammation of the brain and spinal cord.

Usually results from an infection.

What are the causes of Encephalitis?

Viral

• Arthropod-borne viruses

  • Most common

  • Ex) Eastern Equine Encephalitis, West Nile Virus

• Herpes simplex

Bacterial

• Lyme disease

• TB

• Syphilis

Pathology of Encephalitis

Infection triggers inflammatory response.

• Vasodilatation

• Increased capillary permeability (“leaky”)

• Leukocyte infiltration.

The inflammatory process can cause nerve cell degeneration and diffuse brain destruction

• Cerebral edema possible from inflammation.

• Nerve cell degeneration → Liquid necrosis